The object here is to obtain insight into the genetic determination of form. In bacteriophage T4, mutations are known that cause alteration of capsid length but not diameter. Others effect changes of both dimensions. The most extensively studied group consists of the former type, more specifically those mapping in gene 23 (major capsid structural protein). More than 50 independent mutations have all mapped at 8 gene-23 sites, and these are distributed in 3 tight clusters. We suggest that these clusters reflect 3 short segments of the protein whose interactions play decisive roles in controlling capsid length. Although wild-type T4 lysates rarely contain more than 1-2% capsids of abnormal length, stocks of gene-23 ptg mutants frequency contain more than 75%. We will compare the amino acid sequences of normal and mutant gene-23 proteins, expecting to learn what amino acid substitutions cause loss of fidelity in capsid length determination. A complete study of capsid-shape control must include investigating the other genes that play significant roles. Genes 22 and 24 are already known to have such functions, and genetic study of gene-22 mutants has been started. It will be followed by a molecular study. Identification of still unrecognized shape-controlling genes involves isolating gene-23 ptg revertants. Among them, those occurring at genetic sites different from the original mutation are selected. Mapping them will presumably identify genes who products interact with gene-23 protein in length control.